Thats strange, perhaps IL-8 is not best cytokine to look at. In this study IL-8 has a fairly high spread so if the number of tested persons are low one could end up with the opposit result by chance.
Welcome to Phoenix Rising!
Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
To register, simply click the Register button at the top right.
In this thesis, we show that CFS has a biological basis that is detectable in gene expression data better than blood prole and Single Nucleotide Polymorphism (SNP) data. Using random forests, the analysis of gene expression data achieves a prediction accuracy of approximately 89%. We also identify sets of dierentially expressed candidate genes that might contribute to CFS. We show that the integration of data spanning multiple levels of the biological scale might reveal further insights into the understanding of CFS. Using integrated data, we achieve a prediction accuracy of approximately 91%.
Yes, that is what they found:Its nice to see that this paper and dr Kerrs supporting something like a viral pathogen behind CFS
Take a look on IL-5. All PWCFS had higher levels then the controls. Perhaps IL-5 would be the most usefull for diagnostics?
.................... ME/CFS..................... Control...............................
IL-5.. TH2...7.4 (6.3 - 10.0)...........3.8 (3.2 - 5.6)................+ 95
"Applying (ROC) curve analyses, areas under the curves (AUC) for IL-5 (0. 84), LTα (0.77), IL-4 (0.77), IL-12 (0.76) indicated good biomarker potential."
Values in parentheses are 25th and 75th percentiles.
The study linked to was done using the empiric/Reeves criteria (see: 2.2 CAMDA dataset) so unfortunately I have little faith that they were studying CFS patients.Levi, you do come up with "good stuff, man."
This thesis, looking at gene expression data to predict ME/CFS, was in 2007. The author claims accuracy rates of 89% and 91% depending on methodology. Does anyone know if other follow-up work was done on this? Does this tie in with Dr. Kerr?
It looks like they might produce one or more paper looking at this:I don't have any direct evidence, but I think I go through "cytokine storms" at various times.
I'm not sure what triggers them, but I know they make me feel really bad.
Obvious limitations of this study are that the samples represent
a single point in time and a single gender. The parent
protocol, from which the CFS samples were gathered,
is a larger longitudinal study. Subjects are followed over
18 months and sample collection includes times of relative
symptom remission or exacerbation. Completion of
the study will allow the correlation of CFS related symptoms
and other immune markers with the cytokine patterns.
I just reread this, and I"m wondering what those three therapeutic strategies are. Anyone know?Conclusions: Cytokine abnormalities are common in CFS. In this study, 10 of 16 cytokines examined showed good to fair promise as biomarkers.
However, the cytokine changes observed are likely to more indicative of immune activation and inflammation, rather than specific for CFS. As such, they are targets for 3 therapeutic strategies.